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Artículos de revistas sobre el tema "Wound healing Physiology"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 31 de enero de 2023

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1

Strodtbeck, Frances. "Physiology of wound healing." Newborn and Infant Nursing Reviews 1, no. 1 (March 2001): 43–52. http://dx.doi.org/10.1053/nbin.2001.23176.

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2

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology–Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/s0194-5998(10)02297-7.

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3

Silver, I. A. "The physiology of wound healing." Journal of Wound Care 3, no. 2 (March 2, 1994): 106–9. http://dx.doi.org/10.12968/jowc.1994.3.2.106.

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4

Flanagan, M. "The physiology of wound healing." Journal of Wound Care 9, no. 6 (June 2000): 299–300. http://dx.doi.org/10.12968/jowc.2000.9.6.25994.

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5

Rhee, John S., David Hom, and Timothy Lian. "Wound Healing and Flap Physiology." Otolaryngology - Head and Neck Surgery 143, no. 5 (November 2010): 718. http://dx.doi.org/10.1016/j.otohns.2010.09.045.

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6

Young, Alistair, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 29, no. 10 (October 2011): 475–79. http://dx.doi.org/10.1016/j.mpsur.2011.06.011.

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7

Harper, Daniel, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 32, no. 9 (September 2014): 445–50. http://dx.doi.org/10.1016/j.mpsur.2014.06.010.

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8

Singh, Shailendra, Alistair Young, and Clare-Ellen McNaught. "The physiology of wound healing." Surgery (Oxford) 35, no. 9 (September 2017): 473–77. http://dx.doi.org/10.1016/j.mpsur.2017.06.004.

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9

Hunt, Thomas K. "The physiology of wound healing." Annals of Emergency Medicine 17, no. 12 (December 1988): 1265–73. http://dx.doi.org/10.1016/s0196-0644(88)80351-2.

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10

Norris, Susan O’Brien, Barbara Provo, and Nancy A. Stotts. "Physiology of Wound Healing and Risk Factors that Impede the Healing Process." AACN Advanced Critical Care 1, no. 3 (November 1, 1990): 545–52. http://dx.doi.org/10.4037/15597768-1990-3010.

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In the critically ill patient, wound repair can be impeded by processes inherent to the illness, its treatment, and the critical care environment. This vulnerability to wound complications increases patient morbidity and mortality as well as length of stay, resource consumption, and hospital cost. The physiology of wound healing and factors that impede wound repair are discussed. Those factors commonly seen in critical illness include advanced age, diabetes mellitus, compromised immunocompetence, inadequate perfusion, and oxygenation, infection, malnutrition, obesity, and preoperative illness.

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11

Clancy, John, Andrew McVicar, and Damian Muncaster. "The Physiology of Wound Healing and Wound Assessment." British Journal of Perioperative Nursing (United Kingdom) 11, no. 8 (August 2001): 362–70. http://dx.doi.org/10.1177/175045890101100805.

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12

Phillips, Steven J. "Physiology of Wound Healing and Surgical Wound Care." ASAIO Journal 46, no. 6 (November 2000): S2—S5. http://dx.doi.org/10.1097/00002480-200011000-00029.

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13

Lloyd-Jones, Menna. "Tissue viability: the physiology of wound healing." British Journal of Healthcare Assistants 1, no. 4 (July 2007): 181–84. http://dx.doi.org/10.12968/bjha.2007.1.4.24265.

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14

Gantwerker, Eric A., and David B. Hom. "Skin: Histology and Physiology of Wound Healing." Facial Plastic Surgery Clinics of North America 19, no. 3 (August 2011): 441–53. http://dx.doi.org/10.1016/j.fsc.2011.06.009.

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15

Honrado, Carlo P., and Craig S. Murakami. "Wound Healing and Physiology of Skin Flaps." Facial Plastic Surgery Clinics of North America 13, no. 2 (May 2005): 203–14. http://dx.doi.org/10.1016/j.fsc.2004.11.007.

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16

Gantwerker, Eric A., and David B. Hom. "Skin: Histology and Physiology of Wound Healing." Clinics in Plastic Surgery 39, no. 1 (January 2012): 85–97. http://dx.doi.org/10.1016/j.cps.2011.09.005.

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17

Childress, Beverly B., and Joyce K. Stechmiller. "Role of Nitric Oxide in Wound Healing." Biological Research For Nursing 4, no. 1 (July 2002): 5–15. http://dx.doi.org/10.1177/1099800402004001002.

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Chronic wounds mainly affect elderly individuals and persons with comorbid diseases due to a compromised immune status. An age-related decline in immune function deters proper healing of wounds in an orderly and timely manner. Thus, older adults with 1 or more concomitant illnesses are more likely to experience and suffer from a nonhealing wound, which may drastically decrease their quality of life and financial resources. Novel therapies in wound care management rely heavily on our current knowledge of wound healing physiology. It is well established that normal wound healing occurs sequentia

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18

Giglio, James A., A. Omar Abubaker, and Robert F. Diegelmann. "PHYSIOLOGY OF WOUND HEALING OF SKIN AND MUCOSA." Oral and Maxillofacial Surgery Clinics of North America 8, no. 4 (November 1996): 457–65. http://dx.doi.org/10.1016/s1042-3699(20)30918-3.

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19

Witte, Maria B., and Adrian Barbul. "Arginine physiology and its implication for wound healing." Wound Repair and Regeneration 11, no. 6 (November 2003): 419–23. http://dx.doi.org/10.1046/j.1524-475x.2003.11605.x.

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20

DYSON, MARY. "Advances in wound healing physiology: the comparative perspective." Veterinary Dermatology 8, no. 4 (December 1997): 227–33. http://dx.doi.org/10.1111/j.1365-3164.1997.tb00268.x.

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21

Teller, Paige, and Therese K. White. "The Physiology of Wound Healing: Injury Through Maturation." Surgical Clinics of North America 89, no. 3 (June 2009): 599–610. http://dx.doi.org/10.1016/j.suc.2009.03.006.

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22

Teller, Paige, and Therese K. White. "The Physiology of Wound Healing: Injury Through Maturation." Perioperative Nursing Clinics 6, no. 2 (June 2011): 159–70. http://dx.doi.org/10.1016/j.cpen.2011.04.001.

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23

Rodrigues, Melanie, Nina Kosaric, Clark A. Bonham, and Geoffrey C. Gurtner. "Wound Healing: A Cellular Perspective." Physiological Reviews 99, no. 1 (January 1, 2019): 665–706. http://dx.doi.org/10.1152/physrev.00067.2017.

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Wound healing is one of the most complex processes in the human body. It involves the spatial and temporal synchronization of a variety of cell types with distinct roles in the phases of hemostasis, inflammation, growth, re-epithelialization, and remodeling. With the evolution of single cell technologies, it has been possible to uncover phenotypic and functional heterogeneity within several of these cell types. There have also been discoveries of rare, stem cell subsets within the skin, which are unipotent in the uninjured state, but become multipotent following skin injury. Unraveling the rol

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24

Thiruvoth, FrijiMeethale, DeviPrasad Mohapatra, DineshKumar Sivakumar, RaviKumar Chittoria, and Vijayaraghavan Nandhagopal. "Current concepts in the physiology of adult wound healing." Plastic and Aesthetic Research 2, no. 5 (2015): 250. http://dx.doi.org/10.4103/2347-9264.158851.

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25

Ascenção, A. M. S., H. V. D. Boer, T. B. Paiva, and L. M. Vianna. "P.89 Physiology of vitamin D3 on wound healing." Clinical Nutrition 17 (August 1998): 53. http://dx.doi.org/10.1016/s0261-5614(98)80245-8.

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26

Russell, Linda. "Understanding physiology of wound healing and how dressings help." British Journal of Nursing 9, no. 1 (January 13, 2000): 10–21. http://dx.doi.org/10.12968/bjon.2000.9.1.6406.

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27

Hu, Michael S., Mimi R. Borrelli, H. Peter Lorenz, Michael T. Longaker, and Derrick C. Wan. "Mesenchymal Stromal Cells and Cutaneous Wound Healing: A Comprehensive Review of the Background, Role, and Therapeutic Potential." Stem Cells International 2018 (2018): 1–13. http://dx.doi.org/10.1155/2018/6901983.

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Cutaneous wound repair is a highly coordinated cascade of cellular responses to injury which restores the epidermal integrity and its barrier functions. Even under optimal healing conditions, normal wound repair of adult human skin is imperfect and delayed healing and scarring are frequent occurrences. Dysregulated wound healing is a major concern for global healthcare, and, given the rise in diabetic and aging populations, this medicoeconomic disease burden will continue to rise. Therapies to reliably improve nonhealing wounds and reduce scarring are currently unavailable. Mesenchymal stromal

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28

Auger, F. A., D. Lacroix, and L. Germain. "Skin Substitutes and Wound Healing." Skin Pharmacology and Physiology 22, no. 2 (2009): 94–102. http://dx.doi.org/10.1159/000178868.

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29

McElvain, Kelly, Joshua Klister, Alessandra Ebben, Sandeep Gopalakrishnan, and Mahsa Dabagh. "Impact of Wound Dressing on Mechanotransduction within Tissues of Chronic Wounds." Biomedicines 10, no. 12 (November 30, 2022): 3080. http://dx.doi.org/10.3390/biomedicines10123080.

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Chronic wounds are significant public health problems impacting the health-related quality of individuals’ lives (due to disability, decreased productivity, and loss of independence) and an immense economic burden to healthcare systems around the world. In this study, our main objective is to investigate how mechanotransduction can impact the healing process in chronic wounds. We have developed new three-dimensional models of wound tissue to study the distribution of forces within these tissues exerted by wound dressings with different characteristics. The roles of mechanical forces on wound h

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30

Branski, Ryan C. "Perioperative Voice Recovery: A Wound-Healing Perspective." Perspectives on Voice and Voice Disorders 23, no. 2 (July 2013): 42–46. http://dx.doi.org/10.1044/vvd23.2.42.

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To describe the wound healing process through an oversimplified graphic, a classic cartoon in a Dermatology Clinics textbook shows a Volkswagen Beetle, with the license plate TRAUMA that has driven through a wooden fence, leaving both a substantive hole in the fence and piles of broken wooden planks. The obvious priority would be to rebuild the fence so that it is identical to its pretrauma state. This analogy and accompanying graphic provide a framework for a unique perspective on wound healing. For the sake of simplicity, let us assume that the vocal fold is a fence, and instead of a Volkswa

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31

Scott, Christopher, James Bonner, Danqing Min, Philip Boughton, Rebecca Stokes, Kuan Minn Cha, Stacey N. Walters, et al. "Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing." American Journal of Physiology-Cell Physiology 307, no. 4 (August 15, 2014): C349—C357. http://dx.doi.org/10.1152/ajpcell.00306.2013.

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Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that binds to partners to mediate responses to environmental signals. To investigate its role in the innate immune system, floxed ARNT mice were bred with lysozyme M-Cre recombinase animals to generate lysozyme M-ARNT (LAR) mice with reduced ARNT expression. Myeloid cells of LAR mice had altered mRNA expression and delayed wound healing. Interestingly, when the animals were rendered diabetic, the difference in wound healing between the LAR mice and their littermate controls was no longer present, suggesting that de

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32

Grasso, Silvina, Julio A. Hernández, and Silvia Chifflet. "Roles of wound geometry, wound size, and extracellular matrix in the healing response of bovine corneal endothelial cells in culture." American Journal of Physiology-Cell Physiology 293, no. 4 (October 2007): C1327—C1337. http://dx.doi.org/10.1152/ajpcell.00001.2007.

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It has classically been accepted that the healing of narrow wounds in epithelia occurs by the formation of a contractile actin cable, while wide wounds are resurfaced by lamellipodia-dependent migration of border cells into the denuded area. To further investigate the general validity of this idea, we performed systematic experiments of the roles of wound geometry, wound size, and extracellular matrix (ECM) in wound healing in monolayers of bovine corneal endothelial cells, a system shown here to predominantly display any of the two healing mechanisms according to the experimental conditions.

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33

Potekaev, Nikolai N., Olga B. Borzykh, German V. Medvedev, Denis V. Pushkin, Marina M. Petrova, Artem V. Petrov, Diana V. Dmitrenko, Elena I. Karpova, Olga M. Demina, and Natalia A. Shnayder. "The Role of Extracellular Matrix in Skin Wound Healing." Journal of Clinical Medicine 10, no. 24 (December 18, 2021): 5947. http://dx.doi.org/10.3390/jcm10245947.

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Impaired wound healing is one of the unsolved problems of modern medicine, affecting patients’ quality of life and causing serious economic losses. Impaired wound healing can manifest itself in the form of chronic skin wounds or hypertrophic scars. Research on the biology and physiology of skin wound healing disorders is actively continuing, but, unfortunately, a single understanding has not been developed. The attention of clinicians to the biological and physiological aspects of wound healing in the skin is necessary for the search for new and effective methods of prevention and treatment of

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34

Rybinski, Brad, Janusz Franco-Barraza, and Edna Cukierman. "The wound healing, chronic fibrosis, and cancer progression triad." Physiological Genomics 46, no. 7 (April 1, 2014): 223–44. http://dx.doi.org/10.1152/physiolgenomics.00158.2013.

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For decades tumors have been recognized as “wounds that do not heal.” Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct si

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35

Quirós, Miguel, and Asma Nusrat. "Contribution of Wound-Associated Cells and Mediators in Orchestrating Gastrointestinal Mucosal Wound Repair." Annual Review of Physiology 81, no. 1 (February 10, 2019): 189–209. http://dx.doi.org/10.1146/annurev-physiol-020518-114504.

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The gastrointestinal mucosa, structurally formed by the epithelium and lamina propria, serves as a selective barrier that separates luminal contents from the underlying tissues. Gastrointestinal mucosal wound repair is orchestrated by a series of spatial and temporal events that involve the epithelium, recruited immune cells, resident stromal cells, and the microbiota present in the wound bed. Upon injury, repair of the gastrointestinal barrier is mediated by collective migration, proliferation, and subsequent differentiation of epithelial cells. Epithelial repair is intimately regulated by a

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36

Becirovic-Agic, Mediha, Upendra Chalise, Mira Jung, Jocelyn R. Rodriguez-Paar, Shelby R. Konfrst, Elizabeth R. Flynn, Jeffrey D. Salomon, Michael E. Hall, and Merry L. Lindsey. "Faster skin wound healing predicts survival after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 322, no. 4 (April 1, 2022): H537—H548. http://dx.doi.org/10.1152/ajpheart.00612.2021.

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Faster skin wound healers had more efficient cardiac healing after myocardial infarction (MI). Two plasma proteins at D3 MI, EAF1 and A2M, predicted MI death in 66% of cases. ApoD regulated both skin and cardiac wound healing in male mice by promoting inflammation. The skin was a mirror to the heart and common pathways linked wound healing across organs.

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37

Roy, Sashwati, Savita Khanna, Cameron Rink, Sabyasachi Biswas, and Chandan K. Sen. "Characterization of the acute temporal changes in excisional murine cutaneous wound inflammation by screening of the wound-edge transcriptome." Physiological Genomics 34, no. 2 (July 2008): 162–84. http://dx.doi.org/10.1152/physiolgenomics.00045.2008.

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This work represents a maiden effort to systematically screen the transcriptome of the healing wound-edge tissue temporally using high-density GeneChips. Changes during the acute inflammatory phase of murine excisional wounds were characterized histologically. Sets of genes that significantly changed in expression during healing could be segregated into the following five sets: up-early (6–24 h; cytokine-cytokine receptor interaction pathway), up-intermediary (12–96 h; leukocyte-endothelial interaction pathway), up-late (48–96 h; cell-cycle pathway), down-early (6–12 h; purine metabolism) and

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38

Chen, Jing, Yu Chen, Yajie Chen, Zicheng Yang, Bo You, Ye Chun Ruan та Yizhi Peng. "Epidermal CFTR Suppresses MAPK/NF-κB to Promote Cutaneous Wound Healing". Cellular Physiology and Biochemistry 39, № 6 (2016): 2262–74. http://dx.doi.org/10.1159/000447919.

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Background: CFTR is implicated in cutaneous wound healing although the underlying mechanisms are not fully understood. In other cell types, CFTR is reported to regulate MAPK/ NF-κB signaling. We undertook the present study to explore a possible role of CFTR in regulating MAPK/NF-κB during cutaneous wound healing. Methods&amp; Results: The splint-excisional and incisional wound healing models were used in CFTR mutant (DF508) mice. The cell-scratch model was used in a human keratinocyte line, HaCaT, in conjunction with CFTR knockdown or overexpression. The epidermal inflammation, keratinocyt

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39

Guo, Jianming, Haidi Hu, Jolanta Gorecka, Hualong Bai, Hao He, Roland Assi, Toshihiko Isaji, et al. "Adipose-derived mesenchymal stem cells accelerate diabetic wound healing in a similar fashion as bone marrow-derived cells." American Journal of Physiology-Cell Physiology 315, no. 6 (December 1, 2018): C885—C896. http://dx.doi.org/10.1152/ajpcell.00120.2018.

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We have previously shown that bone marrow-derived mesenchymal stem cells (BMSC) accelerate wound healing in a diabetic mouse model. In this study, we hypothesized that adipose tissue-derived stem cells (ADSC), cells of greater translational potential to human therapy, improve diabetic wound healing to a similar extent as BMSC. In vitro, the characterization and function of murine ADSC and BMSC as well as human diabetic and nondiabetic ADSC were evaluated by flow cytometry, cell viability, and VEGF expression. In vivo, biomimetic collagen scaffolds containing murine ADSC or BMSC were used to tr

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40

Roy, Sashwati, and Chandan K. Sen. "MiRNA in innate immune responses: novel players in wound inflammation." Physiological Genomics 43, no. 10 (May 2011): 557–65. http://dx.doi.org/10.1152/physiolgenomics.00160.2010.

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Chronic wounds represent a major and rising socioeconomic threat affecting over 6.5 million people in the United States costing in excess of US $25 billion annually. Wound healing is a physiological response to injury that is conserved across tissue systems. In humans, wounding is followed by instant response aimed at hemostasis, which in turn provides the foundation for inflammatory processes that closely follow. Inflammation is helpful and a prerequisite for healing as long as it is mounted and resolved in a timely manner. Chronic inflammation derails the healing cascade resulting in impaire

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41

Wietecha, Mateusz S., Lin Chen, Matthew J. Ranzer, Kimberly Anderson, Chunyi Ying, Tarun B. Patel, and Luisa A. DiPietro. "Sprouty2 downregulates angiogenesis during mouse skin wound healing." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 2 (February 2011): H459—H467. http://dx.doi.org/10.1152/ajpheart.00244.2010.

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Angiogenesis is regulated by signals received by receptor tyrosine kinases such as vascular endothelial growth factor receptors. Mammalian Sprouty (Spry) proteins are known to function by specifically antagonizing the activation of the mitogen-activated protein kinase signaling pathway by receptor tyrosine kinases, a pathway known to promote angiogenesis. To examine the role of Spry2 in the regulation of angiogenesis during wound repair, we used a model of murine dermal wound healing. Full-thickness excisional wounds (3 mm) were made on the dorsum of anesthetized adult female FVB mice. Samples

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42

Yang, J., L. W. Tyler, R. B. Donoff, B. Song, A. J. Torio, G. T. Gallagher, T. Tsuji, et al. "Salivary EGF regulates eosinophil-derived TGF-alpha expression in hamster oral wounds." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 1 (January 1, 1996): G191—G202. http://dx.doi.org/10.1152/ajpgi.1996.270.1.g191.

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Using hamster as an oral wound healing model, we examined eosinophils and their expression of transforming growth factor-alpha (TGF-alpha) and transforming growth factor-beta 1 (TGF-beta 1). Oral wounds healed approximately two times faster than their cutaneous counterparts. Eosinophils infiltrated prominently into oral wounds; however, unlike the dual expression of TGF-alpha and TGF-beta 1 in skin wounds, oral wound-associated eosinophils expressed TGF-beta 1, but not TGF-alpha. Because saliva is present in oral environments and contains epidermal growth factor (EGF) and TGF-alpha, sialoadene

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43

Nouvong, Aksone, Aaron M. Ambrus, Ellen R. Zhang, Lucas Hultman, and Hilary A. Coller. "Reactive oxygen species and bacterial biofilms in diabetic wound healing." Physiological Genomics 48, no. 12 (December 1, 2016): 889–96. http://dx.doi.org/10.1152/physiolgenomics.00066.2016.

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Chronic wounds are a common and debilitating complication for the diabetic population. It is challenging to study the development of chronic wounds in human patients; by the time it is clear that a wound is chronic, the early phases of wound healing have passed and can no longer be studied. Because of this limitation, mouse models have been employed to better understand the early phases of chronic wound formation. In the past few years, a series of reports have highlighted the importance of reactive oxygen species and bacterial biofilms in the development of chronic wounds in diabetics. We rev

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44

Radek, Katherine A., Lisa A. Baer, Jennifer Eckhardt, Luisa A. DiPietro, and Charles E. Wade. "Mechanical unloading impairs keratinocyte migration and angiogenesis during cutaneous wound healing." Journal of Applied Physiology 104, no. 5 (May 2008): 1295–303. http://dx.doi.org/10.1152/japplphysiol.00977.2007.

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Although initially thought to improve an individual's ability to heal, mechanical unloading promoted by extended periods of bed rest has emerged as a contributing factor to delayed or aberrant tissue repair. Using a rat hindlimb unloading (HLU) model of hypogravity, we mimicked some aspects of physical inactivity by removing weight-bearing loads from the hindlimbs and producing a systemic cephalic fluid shift. This model simulates bed rest in that the animal undergoes physiological adaptations, resulting in a reduction in exercise capability, increased frequency of orthostatic intolerance, and

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45

Fox, Miriam D. "Wound Care in the Neonatal Intensive Care Unit." Neonatal Network 30, no. 5 (2011): 291–303. http://dx.doi.org/10.1891/0730-0832.30.5.291.

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The skin is a vital organ with key protective functions. Infants in the NICU are at risk for skin injury because of developmental immaturity and intensive care treatments. When skin injury occurs, the neonatal nurse is challenged to provide wound care to optimize functional and cosmetic healing. Optimal wound care requires basic knowledge of the mechanisms of injury, physiology of wound healing, host factors affecting wound healing, and wound assessment. This knowledge provides the basis for determining appropriate wound treatment, including dressing selection. Attention to pain issues associa

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46

Grzesik, Wojciech J., and A. S. Narayanan. "Cementum and Periodontal Wound Healing and Regeneration." Critical Reviews in Oral Biology & Medicine 13, no. 6 (November 2002): 474–84. http://dx.doi.org/10.1177/154411130201300605.

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The extracellular matrix (ECM) of cementum resembles other mineralized tissues in composition; however, its physiology is unique, and it contains molecules that have not been detected in other tissues. Cementum components influence the activities of periodontal cells, and they manifest selectivity toward some periodontal cell types over others. In light of emerging evidence that the ECM determines how cells respond to environmental stimuli, we hypothesize that the local environment of the cementum matrix plays a pivotal role in maintaining the homeostasis of cementum under healthy conditions.

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47

Mroz, Magdalena S., Natalia K. Lajczak, Bridie J. Goggins, Simon Keely, and Stephen J. Keely. "The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 3 (March 1, 2018): G378—G387. http://dx.doi.org/10.1152/ajpgi.00435.2016.

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The intestinal epithelium constitutes an innate barrier which, upon injury, undergoes self-repair processes known as restitution. Although bile acids are known as important regulators of epithelial function in health and disease, their effects on wound healing processes are not yet clear. Here we set out to investigate the effects of the colonic bile acids, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA), on epithelial restitution. Wound healing in T84 cell monolayers grown on transparent, permeable supports was assessed over 48 h with or without bile acids. Cell migration was measured

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48

Mirastschijski, Ursula, Dongsheng Jiang, and Yuval Rinkevich. "Genital Wound Repair and Scarring." Medical Sciences 10, no. 2 (April 18, 2022): 23. http://dx.doi.org/10.3390/medsci10020023.

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Skin wound repair has been the central focus of clinicians and scientists for almost a century. Insights into acute and chronic wound healing as well as scarring have influenced and ameliorated wound treatment. Our knowledge of normal skin notwithstanding, little is known of acute and chronic wound repair of genital skin. In contrast to extra-genital skin, hypertrophic scarring is uncommon in genital tissue. Chronic wound healing disorders of the genitals are mostly confined to mucosal tissue diseases. This article will provide insights into the differences between extra-genital and genital sk

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Zhou, Xiangjun, Wei Zhang, Qisheng Yao, Hao Zhang, Guie Dong, Ming Zhang, Yutao Liu, Jian-Kang Chen, and Zheng Dong. "Exosome production and its regulation of EGFR during wound healing in renal tubular cells." American Journal of Physiology-Renal Physiology 312, no. 6 (June 1, 2017): F963—F970. http://dx.doi.org/10.1152/ajprenal.00078.2017.

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Kidney repair following injury involves the reconstitution of a structurally and functionally intact tubular epithelium. Growth factors and their receptors, such as EGFR, are important in the repair of renal tubules. Exosomes are cell-produced small (~100 nm in diameter) vesicles that contain and transfer proteins, lipids, RNAs, and DNAs between cells. In this study, we examined the relationship between exosome production and EGFR activation and the potential role of exosome in wound healing. EGFR activation occurred shortly after scratch wounding in renal tubular cells. Wound repair after scr

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Kung, Hsiu-Ni, Mei-Jun Yang, Chi-Fen Chang, Yat-Pang Chau та Kuo-Shyan Lu. "In vitro and in vivo wound healing-promoting activities of β-lapachone". American Journal of Physiology-Cell Physiology 295, № 4 (жовтень 2008): C931—C943. http://dx.doi.org/10.1152/ajpcell.00266.2008.

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Impaired wound healing is a serious problem for diabetic patients. Wound healing is a complex process that requires the cooperation of many cell types, including keratinocytes, fibroblasts, endothelial cells, and macrophages. β-Lapachone, a natural compound extracted from the bark of the lapacho tree ( Tabebuia avellanedae), is well known for its antitumor, antiinflammatory, and antineoplastic effects at different concentrations and conditions, but its effects on wound healing have not been studied. The purpose of the present study was to investigate the effects of β-lapachone on wound healing

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